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152

 

 

 

 

 

Practical Urology: EssEntial PrinciPlEs and PracticE

physiological effects of sodium and potassium

Absorptive Hypercalciuria

cations by showing that potassium alkali reduces

There is currently no treatment program which

urinary calcium while sodium alkali does

is capable of correcting the basic abnormality of

not.46,47 Therefore, it is advisable to generally

recommend dietary salt reduction especially

absorptivehypercalciuriaTypeI(AHI).Although

sodium cellulose phosphate had been used in

among calcium stone producers.

the past as a nonabsorbable ion exchange resin

Similarly, we recommend restriction of ani-

to bind calcium and inhibits its absorption, this

mal protein intake in stone-forming patients.

medication is no longer available.

Studies conducted under controlled clinical lab-

 

oratory settings have demonstrated the risk of

 

hypercalciuria and hyperuricosuria as a result

Thiazide

of diet high in animal protein.48-50 These find-

Thiazide is not considered a selective therapy

ings were further supported by epidemiologic

studies that found a positive correlation between

for absorptive hypercalciuria, since it does not

diets rich in protein and the high prevalence of

decrease intestinal calcium absorption in this

stone disease.51,52

condition. However, this drug has been widely

Later studies have shown the effect of dietary

used to treat absorptive hypercalciuria.

protein restriction on decreasing the levels of

Potassium supplementation should be emp-

calcium, phosphate, oxalate, and uric acid while

loyed when using thiazide therapy in order to

increasing the levels of urinary citrate.53,54

prevent hypokalemia and a decrease in urinary

 

 

citrate excretion. A typical treatment program

Restricted Oxalate Diet

might include chlorthalidone 25 mg/day with

potassium citrate 20 mEq twice/day.

 

 

Although this recommendation may be pro-

In absorptive hypercalciuria Type II, no spe-

vided to all stone patients, it is most useful for

cific drug treatment may be necessary since the

patients with enteric hyperoxaluria or underly-

physiologic defect is not as severe as in absorp-

ing bowel abnormalities.55 Traditional foods

tive hypercalciuria Type I. A low calcium intake

rich in oxalate includes: black tea, cocoa, spin-

(400–600 mg/day) and high fluid intake (suffi-

ach, mustard greens, pokeweed, swiss chard,

cient to achieve a minimum urine output of

beets,rhubarb,okra,chocolate,nuts,wheat germ,

greater than 2 L/day) would seem ideally indi-

soy crackers, pepper.

cated.

Conservative Measures

Orthophosphate

Under conservative management, the patient should be followed within 3–4 months with current imaging, a basic metabolic panel, and 24 h urine sample collection as described above. Provided the baseline abnormalities have been corrected, an appointment should be re-sched- uled in 6–12 months with repeated 24 h urine testing.

Selective Medical Therapy

This entity is kept for persistent metabolic disorders despite proper conservative management. Various regimens currently exist in the market for treating resistant metabolic disturbances and are given in Table 11.3. Drug efficacy and dosage modifications should be monitored via the 24 h urine collection.

Orthophosphate (neutral or alkaline salt of sodium and/or potassium, 0.5 g phosphorus three to four times/day) has been shown to inhibit 1,25-(OH)2D synthesis and reduce urinary calcium excretion. Moreover, there is some preliminary evidence that this treatment restores normal intestinal calcium absorption. This medication may be particularly indicated in absorptive hypercalciuria Type III; however, it is contraindicated in nephrolithiasis complicated by urinary tract infection.

Renal Hypercalciuria

Thiazide is ideally indicated for the treatment of renal hypercalciuria. This diuretic has been shown to correct the renal leak of calcium by augmenting calcium reabsorption in the distal tubule and by causing extracellular volume

153

MEtabolic EvalUation and MEdical ManagEMEnt of stonE disEasE

Table 11.3. stone management – medication summary

 

 

 

Medication

Indications

Side effects

Dose

Other notes

thiazide

Hypercalciuria

Hypokalemia

chlorthalidone

High sodium intake

 

(absorptive type i, ii;

 

25–50 mg

will offset effect of

 

renal)

 

Po qd

thiazide

 

Hyperoxaluria (primary,

 

indapamide:

often administered

 

idiopathic)

 

1.25 mg

with K-citrate or

 

 

 

Po qd

amiloride to

 

 

 

 

counter hypo-

 

 

 

 

kalemic effects

 

 

 

 

often administered

 

 

 

 

with K-citrate to

 

 

 

 

counter acidotic

 

 

 

 

effects

orthophosphate

Hypercalciuria

gi intolerance

Each tab has

side effect profile

 

(absorptive)

 

250 mg Phos

makes this second

 

 

 

1–2 tabs Po

line if thiazides are

 

 

 

Qid

ineffective

bisphosphonate

Hypercalciuria

Hypocalcemia

alendronate

Ensure PtH normal

 

(resorptive)

rash

5–10 mg Po qd

before starting

 

 

 

medical therapy

 

 

 

 

 

 

gi intolerance

risendronate

 

 

 

 

5 mg Po qd

 

Potassium citrate

Hypercalciuria

gi intolerance

40–90 mEq Po

take with meals to

 

Hyperoxaluria

 

divided bid/tid

avoid gi upset

 

 

 

 

 

gouty diathesis

Hyperkalemia

 

 

 

cystinuria

 

 

 

 

Hypocitraturia

 

 

 

sodium bicarbonate

Hyperoxaluria (enteric)

gi intolerance

650–1,300 mg

 

 

gouty diathesis

alkalosis

Po up to Qid

 

 

 

 

 

distal tubular renal

 

 

 

 

acidosis

 

 

 

 

cystinuria

 

 

 

allopurinol

Hyperuricosuria

rash

300–600 mg

Wait until after acute

 

Hyperuricosemia

Xanthine urolithiasis

Po qd

gouty arthritis

 

 

attack subsides

 

 

 

 

 

 

 

 

before starting

d-penicillamine

cystinuria

Pyridoxine

500–1,000 mg

side effect profile

 

 

deficiency

Po Qid

makes this more of

 

 

rash

 

a second-line

 

 

 

agent

 

 

 

 

 

 

agranulocytosis

 

cheaper than thiola

 

 

leukopenia

 

 

 

 

nephrotic syndrome

 

 

 

 

arthralgia

 

 

(continued)

154

Practical Urology: EssEntial PrinciPlEs and PracticE

Table 11.3. (continued)

 

 

 

 

Medication

Indications

Side effects

Dose

Other notes

thiola

cystinuria

similar to

200–1,200 mg

firstline agent

 

 

penicillamine but

Po divided

 

 

 

less common and

bid - Qid

 

 

 

less severe

 

 

captopril

cystinuria

cough

 

 

renal insufficiency

acetohydroxamic acid

infection-based

anemia

 

nephrolithiasis

rash

 

 

 

 

Hepatotoxicity

 

 

gi upset

 

 

dvt

Pyridoxine

Hyperoxaluria

 

 

(primary)

 

 

cystinuria (if

 

 

penicillamine being

 

 

used)

 

ca supplementation

Hyperoxaluria (enteric)

constipation

Mg gluconate

Hyperoxaluria

gi intolerance

 

(primary)

Hyporeflexia

 

 

 

 

Hypotonia/Muscle

 

 

Paralysis

 

 

Hypotension

 

 

cardiac arrhythmia

bile salt resin

Hyperoxaluria (enteric)

gi intolerance

75–150 mg

Usually thirdline

Po qd

agent

250 mg Po tid/

f/U q 3–4 months

Qid

required on this

 

medication to

 

monitor for side

 

effects

Primary: 200–400

 

Po qd

 

adjunct: 50 mg

 

Po qd

 

1–4 g Po tid with

follow-up urine

meals

collections to avoid

 

hypercalcuria

start at 400 or

side effects usually

420 mg Po qd

seen at very high

and tailor to

doses

response

 

cholestyramine 1–4 g Po tid with meals

depletion and stimulating proximal tubular reabsorption of calcium.These effects are shared by hydrochlorothiazide 50 mg twice/day, chlorthalidone 25 mg/day, or trichlormethiazide 4 mg/day. Potassium citrate supplementation (40–60 mEq/day) is advised, since it has been shown to be effective in averting hypokalemia and in increasing urinary citrate, when administered to patients with calcium nephrolithiasis taking thiazide. Thiazide is contraindicated in primary hyperparathyroidism because of potential aggravation of hypercalcemia.

Primary Hyperparathyroidism

Parathyroidectomy is the optimum treatment for nephrolithiasis of primary hyperparathyroidism. Following removal of abnormal parathyroid tissue, urinary calcium is restored to normal commensurate with a decline in serum concentration of calcium and intestinal absorption. There is no established medical treatment for the nephrolithiasis of primary hyperparathyroidism. Although orthophosphates have been recommended for the disease